DOCSLIB.ORG

Total and Peripheral Blood Flow in Acute Myocardial Infarction

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Total and Peripheral Blood Flow in Acute Myocardial Infarction Br Heart J: first published as 10.1136/hrt.19.1.117 on 1 January 1957. Downloaded from TOTAL AND PERIPHERAL BLOOD FLOW IN ACUTE MYOCARDIAL INFARCTION BY G. de J. LEE From the Department of Medicine, St. Thomas's Hospital Medical School Received December 17, 1955 Acute cardiac infarction is an event that might be expected to produce sudden left ventricular heart failure. Although circulatory collapse is common when myocardial infarction is extensive, the clinical signs of cardiac failure are not often dramatic. Recently, therapy involving intra- arterial or intravenous transfusion of patients with severe shock from myocardial infarction has been used (Epstein and Relman, 1949; Silber et al., 1951; Berman and Akman, 1952; Gootnick and Knox, 1953). Similar treatment of patients with acute left ventricular heart failure would be considered foolhardy. The present study of circulatory events occurring in a group of patients admitted to hospital with acute myocardial infarction was an attempt to investigate these apparent discrepancies. MATERIAL AND METHODS Eleven patients were studied. All gave a typical history of cardiac infarction occurring within a few hours of admission, and all had electrocardiographic evidence confirming myocardial infarction. On http://heart.bmj.com/ admission, eight of the patients had antero-posterior chest tele-radiograms taken as they lay recumbent upon a stretcher in the casualty department. In six patients these X-rays were subsequently compared with similar films taken after recovery. On admission to the ward, all the patients received 1/4 gr. morphine HCl intramuscularly. Half an hour later the skin of the antecubital fossa was anesthetized with 2 per cent xylocaine, and a 1/2 mm. polythene catheter inserted through a needle into the antecubital vein; the tip of the catheter was advanced to the superior vena cava and the mean pressure in this region measured, using a saline manometer. At the same time a second needle was inserted into the brachial artery and the blood pressure recorded using a Hansen capacitance manometer (1949). Pressures were measured with reference on September 23, 2021 by guest. Protected copyright. to the sternal angle. Cardiac output was measured using the Hamilton dye technique, a known volume of dye T1824 being injected via the venous catheter, while rapid small arterial samples were being collected simultaneously (Kopelman and Lee, 1951). The " intrathoracic blood volume " was calculated from the estimated cardiac output and mean dye circulation time. Forearm blood flow was obtained using a venous occlusion plethysmograph filled with water at a temperature of 340 C. Two patients subsequently died: one 14 days after admission, from a secondary coronary thrombosis, and one 9 days after admission, from ventricular fibrillation. The remaining nine readily consented to repeat studies being made following recovery some 4-9 weeks after admission. Seven patients, including the two who died, had additional studies performed 1-13 days after admission. The cardiac output and " intrathoracic blood volume " was compared with similar estimations obtained from a group of normal subjects, a group of patients with left ventricular heart failure, and a third group of patients-who had recovered from left ventricular heart failure, studied previously with Dr. H. Kopelman (1951). RESULTS Clinical Findings. The age of the patients varied from 44 to 64 years. Nine were men and two women. 117 Br Heart J: first published as 10.1136/hrt.19.1.117 on 1 January 1957. Downloaded from 118 G. de J. LEE The clinical findings on admission are shown in Table I and were arbitrarily classified in units: 0 indicated no disability other than pain, while 4 represented severe clinical " shock " manifest by prostration, stupor, a cold sweaty cyanosed skin, and a reduced or imperceptible blood pressure when measured by auscultation. TABLE I CLINICAL STATE OF PATIENTS WITH ACUTE MYOCARDIAL INFARCTION ON ADMISSION TO HOSPITAL Skin Ln t Sw Patient Age Sex aShock0-4" statePa40-4 0-4 J.V.P. creps. Temp. Colour ~~~~~~~~~0-4 L. N. 47 F 0 Anxious 3 Warm Pink 2 Raised 0 J. E. 61 M 0 Alert 2 Warm Pink 0 Raised 0 W. J. 48 M I Dull 3 Cool Pale 2 Not visible 0 G. C. 45 M I Anxious 3 Cool Pale 2 Raised 0 R. F. 45 M 2 Dull 2 Cool Grey 2 Raised 1 C. L. 44 M 2 Anxious 3 Warm Pale 0 Raised 0o H. W. 59 M 3 Dull 2 Cold Grey 2 Raised I W. E. 64 M 3 Dull 2 Cool Grey 3 Raised I W. B. 45 M 3 Dull I Cold Grey 3 Raised 0 *W. H. 64 M 3 Dull 2 Cold Grey 2 Raised 1 *M. T. 57 F 4 Semi- ? Cold Cyanosed 3 Raised I conscious * W. H. died on the 9th day after admission. M. T. died on the 14th day after admission. Four patients qualified for Group 3, two for Group 2, two for Group 1, and two for Group 0. The two patients who died were assessed as Group 3 (Case W. H.) and Group 4 (Case M. T.) risks respectively. Pain was present in all cases and its severity varied; it apparently depended to some extent on the level of consciousness of the individual. Only two patients were not sweating at the time of admission. Heart sounds were usually faint and a triple rhythm was heard in six. No pericardial rub was heard on admis- sion, neither did it develop later in any of the patients. The jugular venous pressure was visible above the http://heart.bmj.com/ sternal angle in all patients except one (W. J.). On admission all the patients were able to lie recumbent without respiratory distress, and none complained of dyspncea. There were isolated scattered crepitations at the lung bases in the Groups 2-4 patients. Pulse Rate (Tables II and III, Fig. 1). On admission the pulse rate amongst the eleven patients ranged from 66 to 123 a minute (average 89 a minute). In seven of the nine who recovered, the pulse rate subsequently fell. The pulse rate varied inversely with the stroke volume in eight of the eleven patients studied, but as an isolated observation it gave little information of the clinical severity of the initial illness or of the stroke volume. Thus W. H. and M. T., who were clinically severely shocked on admission on September 23, 2021 by guest. Protected copyright. and who subsequently died, had pulse rates of 100 and 70 a minute respectively on admission, with stroke volumes of 57 and 71 ml. at that time. In contrast, L. N. and W. J., with no clinical signs of circulatory distress and pulse rates of 108 and 90 a minute on admission, had stroke volumes of 103 and 98 ml. respectively. Blood Pressure (Tables II and III, Fig. 1). The mean blood pressure measured intra-arterially on admis- sion ranged from 78 to 113 mm. Hg (average 98 mm. Hg). No obvious correlation existed between the mean blood pressure at the onset of the illness and the clinical severity of symptoms or the initial cardiac output. Amongst the nine patients who were studied again after recovery, four showed a rise in mean pressure associated with a rise in stroke volume. Three of these patients' pressures rose to hypertensive levels. The remaining five also showed a rise in stroke volume with recovery; this was associated with a fall in mean pressure. The initial clinical state of these patients was less shocked than was the state of the four patients whose mean pressure rose with recovery. Pulse pressure on admission varied between 35 and 70 mm. Hg (average 50 mm. Hg). In six patients the pulse pressure increased following recovery and in three patients the pulse pressure decreased with recovery. The initial mean pressures of the two patients who subsequently died (W. H. and M. T.) were 111 and 87 mm. respectively; the pulse pressures were 54 and 50 mm. Hg respectively. Br Heart J: first published as 10.1136/hrt.19.1.117 on 1 January 1957. Downloaded from BLOOD FLOW IN MYOCARDIAL INFARCTION 119 H .24._ I 00 00 0 0 oN 0 6(666ooooN00 oo6o 66 O 6 6 -I -1 0 00 e 0t W _ C 0 C._ 0t1. - 0-t lltt r- Cl "ot> rv - - - 0- r- -0-0 38ci Cr _- 00 , ._ E.o ° -n m "P- Er$ 8 ci fi t-F o .0 0) 0I o-v A- :- - C ICl l CO o.- E_ 0) 0C .0 - >. x E 00 - ON ZNr r-e N> r;.:cn~~~~~Wx E __ -,0CO I0 .0) -; . ._r I 0 oo 0 N,z > _1 0)~~~~~~W - Cl C - - - *- I0 ^~~ b r- .0) . 0. ~~~ .wt^ >.e 0) I 0 2 - W) ON - N a)_ cl>tn It tn a O t- gO 5n 0 -- -- cO_ >* E ICO C., CO7 CZ N 00 kn,-~~t r- en r- 00 0)r Su x E =i 0)a 0 s.,E-0+- 7om .F C , U' r- cE N) mt r1 . _ -Z-- 0) -1I -I S!. :) ON 2 . 0N00roo- n 0ooCrl - 00 0 I" __- IC.) a http://heart.bmj.com/ 0 -00- 00 O top. M ON W 00 C1 ON 0tN-O - ON ON ON 00 0 000 00 ,-r--ooocl 00000 -l V4 E . 0 to IK0)._. _-99~?999WIe 000 en 00 "0- 0 ON 00 O N- 0 k t (ON m4 g t ________~O0 Nt t O 0t I0 _ E 0)c r-->~ ------~---.- + 0) 100 0 0 I0 0-0 00In ) > + Q0) I ++ +++ _. ___~ on September 23, 2021 by guest.
Load more

Recommended publications
  • Differentiating Between Anxiety, Syncope & Anaphylaxis
    Differentiating between anxiety, syncope & anaphylaxis Dr. Réka Gustafson Medical Health Officer Vancouver Coastal Health Introduction Anaphylaxis is a rare but much feared side-effect of vaccination. Most vaccine providers will never see a case of true anaphylaxis due to vaccination, but need to be prepared to diagnose and respond to this medical emergency. Since anaphylaxis is so rare, most of us rely on guidelines to assist us in assessment and response. Due to the highly variable presentation, and absence of clinical trials, guidelines are by necessity often vague and very conservative. Guidelines are no substitute for good clinical judgment. Anaphylaxis Guidelines • “Anaphylaxis is a potentially life-threatening IgE mediated allergic reaction” – How many people die or have died from anaphylaxis after immunization? Can we predict who is likely to die from anaphylaxis? • “Anaphylaxis is one of the rarer events reported in the post-marketing surveillance” – How rare? Will I or my colleagues ever see a case? • “Changes develop over several minutes” – What is “several”? 1, 2, 10, 20 minutes? • “Even when there are mild symptoms initially, there is a potential for progression to a severe and even irreversible outcome” – Do I park my clinical judgment at the door? What do I look for in my clinical assessment? • “Fatalities during anaphylaxis usually result from delayed administration of epinephrine and from severe cardiac and respiratory complications. “ – What is delayed? How much time do I have? What is anaphylaxis? •an acute, potentially
    [Show full text]
  • CIRCULATORY COLLAPSE - EMERGENCY (ISS MED/3A - ALL/FIN) Page 1 of 2 Pages
    SHOCK - CIRCULATORY COLLAPSE - EMERGENCY (ISS MED/3A - ALL/FIN) Page 1 of 2 pages NOTE The most critical step is identifying and treating the underlying cause. Basic causes of shock are: Anaphylaxis - severe allergic reaction Heart attack Loss of circulating blood volume (bleeding, burns, dehydration) Decompression sickness Venous dilation (allergy, pain, drugs, heat stroke, infection) High or low body temperature SIGNS Pulse - rapid, weak, thready Respiration - shallow, irregular, labored Blood Pressure - low, falling Mental State - confused, sluggish, anxious Eyes - pupils may be dilated Skin - cold, clammy, sweating If no pulse or respiration, perform {CARDIOPULMONARY RESUSCITATION: CPR - EMERGENCY} (SODF: ISS MED: EMERGENCY). 1. Evaluate vital signs and record every 5 minutes every 5 minutes. Time (minutes) 0 5 10 15 20 25 30 ALSP Blood Presssure (ALSP-4) Pulse Respiratory Rate ALSP Temperature (Assessment-4) ALSP Pulse Oximeter (Assessment-3) 2. Unstow and don Non-Sterile Gloves (ALSP Airway-4,5,6). If bleeding, control by applying direct pressure using Gauze Pads (Airway-11). 3. Prevent loss of body heat with clothing, sleeping bag, warm environment. 24 AUG 00 4044.shock.circ.collapse.em.doc SHOCK - CIRCULATORY COLLAPSE - EMERGENCY (ISS MED/3A - ALL/FIN) Page 2 of 2 pages 4. Attach ECG leads. Refer to {CARDIOPULMONARY RESUSCITATION: CPR - ECG DATA STORAGE - EMERGENCY} (SODF: ISS MED: EMERGENCY). 5. Contact Surgeon. 6. If no immediate ground communication available, start IV with 1L bag Normal Saline. Fully open roller clamp assembly to allow maximum flow. Refer to {INJECTIONS - NONPOWERED INTRAVENOUS FLUID INFUSION} (SODF: ISS MED: INJECTIONS/IV). 24 AUG 00 4044.shock.circ.collapse.em.doc.
    [Show full text]
  • Circulatory Collapse During Wound Closure In
    Zhang et al. BMC Anesthesiology (2021) 21:4 https://doi.org/10.1186/s12871-020-01220-6 CASE REPORT Open Access Circulatory collapse during wound closure in spine surgery with an unknown cause: a possible adverse effect of topical application of vancomycin? Xiaoqing Zhang, Wenwen Zhai, Min Li and Xiangyang Guo* Abstract Background: Vancomycin (VCM) is effective in fighting Gram-positive bacteria related severe infections, and topical application of VCM powder is widely used in orthopedic surgery to prevent wound infection. However, VCM could lead to infusion rate-dependent antibody-and complement-independent anaphylaxis reaction by inducing direct release of histamine. Case presentation: We retrospectively analyzed seven cases of severe hypotension and shock during wound closure or immediately after orthopedic surgery with unidentifiable reasons. We found that these cases were all associated with local application of VCM powder during wound closure process. Two patients experienced sudden cardiac arrest. Most of the cases (6/7) with circulatory collapse were discharged without severe sequelae. While one case with application of 3 g VCM developed cardiac arrest and remained in a coma due to hypoxic-hypoxic encephalopathy. The clinical presentations and the time of the shock onset were considered to be related with a VCM induced anaphylaxis reaction. However, as this was a retrospective study, and there was no laboratory examination performed, the conclusion was made upon differential diagnosis based on clinical manifestations and the timing of the shock. Conclusions: Local application of VCM may not be as safe as was once believed and may lead to a related anaphylaxis. As VCM induced infusion-rate dependent, non-IgE mediated anaphylaxisischaracterizedbydelayed occurrence, severe hypotension and even circulatory collapse, surgeons and anesthesiologists should be extra vigilant during and after VCM application.
    [Show full text]
  • Impact of Intra-Aortic Balloon Support on Endothelial Function and Tissue Perfusion Markers in Severe Heart Failure
    Central Journal of Cardiology & Clinical Research Bringing Excellence in Open Access Research Article *Corresponding author Silvia Gelás Lage, Instituto do Coração, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Impact of Intra-Aortic Balloon Universidade de Sao Paulo, Sao Paulo, SP, Brazil, Av. Dr. Enéas de Carvalho Aguiar, 44, 05403-000 - São Support on Endothelial Paulo, SP, Brazil, Tel: (55-11) 26615302; Email: Submitted: 12 September 2018 Accepted: 03 October 2018 Function and Tissue Perfusion Published: 05 October 2018 Copyright Markers in Severe Heart © 2018 Lage et al. OPEN ACCESS Failure Keywords • Intra-aortic balloon pump; Severe heart failure; Antônio A. P. Fagundes Júnior, Liliane Kopel, Claudia Bernoche, Endothelial function; Central venous oxygen saturation; Arteriovenous carbon dioxide gradient; Milena F. Macatrão-Costa, Leonardo N. Lopes, Antonio P. B-type natriuretic peptide Mansur, and Silvia Gelás Lage* Heart Institute, Hospital das Clinicas HCFMUSP, Brazil Abstract Background: The intra-aortic balloon pump (IABP) is a common therapy available for ventricular support in critical cardiac patients. The aim of this study was to characterize the effect of IABP on endothelial function, on serum B-type natriuretic peptide (BNP) levels and on central venous oxygen saturation (ScVO2) and arteriovenous carbon dioxide gradient (∆PCO2) as perfusion tissue markers. Methods and results: Twenty-three patients with severe heart failure, mean age 50±13 years, left ventricular ejection fraction of 22±8% were included. All were on IABP support and the protocol considered 3 conditions: 1) IABP ratio 1:1, 2) IABP ratio 1:3 and 3) IAPB ratio 1:1. The period of time between conditions was 20 minutes.
    [Show full text]
  • Shock and Circulatory Support
    17 Emerg Med J: first published as 10.1136/emj.2003.012450 on 20 December 2004. Downloaded from REVIEW Critical care in the emergency department: shock and circulatory support C A Graham, T R J Parke ............................................................................................................................... Emerg Med J 2005;22:17–21. doi: 10.1136/emj.2003.012450 Effective resuscitation includes the rapid identification and will produce organ failure and, in the context of global hypoperfusion, multiple organ failure correction of an inadequate circulation. Shock is said to be ensues. The aim of resuscitation is to prevent present when systemic hypoperfusion results in severe shock worsening and to restore the circulation to dysfunction of the vital organs. The finding of normal a level that meets the body’s tissue oxygen requirements. haemodynamic parameters, for example blood pressure, Shock can arise through a variety of mechan- does not exclude shock in itself. This paper reviews the isms. Pump failure may be attributable to pathophysiology, resuscitation, and continuing inadequate preload (for example, severe bleed- ing), myocardial failure, or excessive afterload. management of the patient presenting with shock to the Shock can also occur with an adequate or emergency department. increased cardiac output as seen in distributive ........................................................................... shock (for example, septic or anaphylactic shock). Vital tissues remain ischaemic as much of the cardiac output
    [Show full text]
  • Postinduction Paced Pulseless Electrical Activity in a Patient with a History of Oropharyngeal Instrumentation– Induced Reflex Circulatory Collapse
    CASE REPORT Ochsner Journal 16:315–320, 2016 Ó Academic Division of Ochsner Clinic Foundation Postinduction Paced Pulseless Electrical Activity in a Patient With a History of Oropharyngeal Instrumentation– Induced Reflex Circulatory Collapse Ryan J. Kline, MD,1 Ky Pham, MD,1 Carmen L. Labrie-Brown, MD,1 Ken Mancuso, MD,1 Paul LeLorier, MD,2 James Riopelle, MD,1 Alan David Kaye, MD, PhD1 1Department of Anesthesiology, Louisiana State University Health Sciences Center, New Orleans, LA 2Department of Internal Medicine, Louisiana State University Health Sciences Center, New Orleans, LA Background: Reflex hypotension and bradycardia have been reported to occur following administration of several drugs associated with administration of anesthesia and also following a variety of procedural stimuli. Case Report: A 54-year-old postmenopausal female with a history of asystole associated with sedated upper gastrointestinal endoscopy and post–anesthetic-induction tracheal intubation received advanced cardiac resuscitation after insertion of a temporary transvenous pacemaker failed to prevent pulseless electrical activity. The patient’s condition stabilized, and she underwent successful cataract extraction, intraocular lens implantation, and pars plana vitrectomy. Conclusion: Cardiac pacemaker insertion prior to performance of a procedure historically associated with reflex circulatory collapse can be expected to protect a patient from bradycardia but not necessarily hypotension. Keywords: Anesthesia–general, heart arrest, pacemaker–artificial, shock Address correspondence to Alan David Kaye, MD, PhD, Professor and Chairman, Department of Anesthesiology, Louisiana State University Health Sciences Center, 1542 Tulane Ave., Room 656, New Orleans, LA 70112. Tel: (504) 568-2319. Email: [email protected] INTRODUCTION during 2 upper gastrointestinal (GI) endoscopic examina- Reflex hypotension and bradycardia have been reported tions under IV sedation without topical anesthesia.
    [Show full text]
  • UK Comparative Audit of Upper Gastrointestinal Bleeding and the Use of Blood
    British Society of Gastroenterology UUKK CCoommppaarraattiivvee AAuuddiitt ooff UUppppeerr GGaassttrrooiinntteessttiinnaall BBlleeeeddiinngg aanndd tthhee UUssee ooff BBlloooodd DDeecceemmbbeerr 2 2000077 St. Elsewhere's Hospital National Comparative Audit of Blood Transfusion TABLE OF CONTENTS Acknowledgements Executive summary 4 Introduction 9 Why is this audit necessary? 9 Aims 9 What does this audit want to report? 10 What does this report include? 10 Who are the principal stakeholders? 10 Methods How were NHS trusts recruited? 11 Nature and size of the case sample for this audit 11 Pilot 11 Audit standards and criteria 11 Data collection 12 Audit report 12 How to read this report 13 The 1993/4 audit of acute upper gastrointestinal haemorrhage 14 Initial results of the UK audit of UGI bleeding and the use of blood 2007 15 Section 1 Principal Findings 17 Section 2 Organisational of Care 21 Section 3 Presentation and Initial care 27 Section 4 Patient Descriptors 33 Section 5 Endoscopy 35 Section 6 Additional Medical Management 43 Section 7 Surgery and Radiology 45 Section 8 Blood Transfusion 48 Section 9 Outcomes 52 Recommendations 54 Action Points 55 Discussion 56 Conclusions 58 References 59 Appendices 1 Participating hospitals i 2 Audit standards vii 3 Rockall score calculator xi 4 Audit questionnaires xii St. Elsewhere s Hospital 2 Acknowledgements We wish to thank all those who have participated in the UK Comparative Audit of Upper Gastrointestinal Bleeding and the Use of Blood. We recognise that this audit required an enormous amount of time and effort from many staff in each participating hospital, and are extremely grateful to everyone who took part for providing what we hope will be useful, meaningful data both at local and national level.
    [Show full text]
  • Cardiac Arrest During Anesthesia W
    130 Vol. 76, No. 3 Cardiac Arrest During Anesthesia W. H. CASSELS, M.D., San Mateo, and NYLA R. ELNES, M.D., Montreal, Canada circumstances, respiratory arrest may persist from SUMMARY perhaps two to twelve minutes before irreversible In cases of acute cardiac arrest from tran- damage results, because the oxygen in the lungs and sient or reversible causes resuscitation is a blood acts as a reservoir. On the other hand, cardiac distinct possibility. Prompt action is of the arrest will probably result in some irreversible dam- utmost importance. age in from two to four minutes. To counteract res- The sequelae of cardiac arrest will depend piratory arrest by artificial respiration requires only on the degree of anoxia that has developed moments because the respiratory mechanism is ac- and the amount of irreversible damage to cessible. To counteract circulatory arrest by man- brain tissue. Efficient manual artificial circu- ual circulation is likely to require minutes. The lation, begun immediately, can prevent such margin of safety in this condition is much narrower. damage. It is fairly obvious that if the heart fails because Four cases of cardiac arrest are described. of irreversible contributing circumstances such as Sudden circulatory collapse, which may or severe hemorrhage, shock, or embolus, efforts at may not imply cardiac arrest, is not uncom- cardiac resuscitation are well-nigh hopeless. On the mon during surgical procedures. Usually the other hand, in cases of acute cardiac arrest from patient recovers quickly when treatment is transient or reversible causes, resuscitation is a dis- prompt. tinct possibility and any restorative measure, no matter how drastic, is justifiable.
    [Show full text]
  • Trauma and Heart Disease
    Case Western Reserve Law Review Volume 5 Issue 2 Article 3 1954 Trauma and Heart Disease Alan R. Moritz Follow this and additional works at: https://scholarlycommons.law.case.edu/caselrev Part of the Law Commons Recommended Citation Alan R. Moritz, Trauma and Heart Disease, 5 W. Rsrv. L. Rev. 133 (1954) Available at: https://scholarlycommons.law.case.edu/caselrev/vol5/iss2/3 This Article is brought to you for free and open access by the Student Journals at Case Western Reserve University School of Law Scholarly Commons. It has been accepted for inclusion in Case Western Reserve Law Review by an authorized administrator of Case Western Reserve University School of Law Scholarly Commons. 1954] Trauma and Heart Disease by Alan R. Moritz WITH LEGAL ANNOTATIONS BY OLIVER SCHROEDER, JR.* D IFFERENCES of opinion in respect to the part played by trauma or stress in the causation of heart disease or in the causation of the failure of the diseased heart are responsible for an enormous volume of litigation. It is dear from reviewing the evidence presented before workman's compen- sation boards and trial courts in such cases that many attorneys know too little about the causal rela- tionships that may or may not exist and that many AUTHOR (B.S., 1920, M.A., 1921, M.D., TiM of 1923, University of Nebraska) is Professor Pathology and Director of the Institute of Path- doctors are insufficiently ology at Western Reserve University. His writ- critical in distinguishing ings have appeared in many legal and medical between medical possi- journals. bility and medical proba- bility.
    [Show full text]
  • Needle Decompression for Tension Pneumothorax: Clinical Correlation with Catheter Length Can J Surg
    INTERNATIONAL TRAUMA LIFE SUPPORT NEEDLE DECOMPRESSION OF TENSION PNEUMOTHORAX Roy Alson, MD, PhD, FACEP, FAAEM and Sabina Braithwaite, MD, MPH, FACEP The guidelines and references contained in this document are current as of the date of publication and in no way replace physician medical oversight. INTRODUCTION The purpose of this document is to update International Trauma Life Support (ITLS) instructors and providers of the position of ITLS in regard to the needle decompression of tension pneumothorax. The seventh edition of the ITLS Provider manual includes additional locations at which a needle decompression of a tension pneumothorax can be carried out beyond the traditional anterior location of the 2nd intercostal space in the mid-clavicular line. A number of other texts, including several used in the tactical medical environment, recommend performing decompression at either the 3rd or 4th intercostal space laterally. These apparently conflicting recommendations have led to confusion on the part of some ITLS instructors and providers with respect to the proper location for needle chest decompression of a tension pneumothorax. BACKGROUND A tension pneumothorax results when air enters the pleural space and is under pressure so that it causes the lung on the affected side to collapse. As a result, the lung is not able to exchange air with the environment and this leads to hypoventilation and hypoxemia. As the pressure rises in the affected hemithorax, the mediastinum can be shifted away from the side of injury and this can cause the vena cava to be compressed. As a result, little to no blood flows back into the heart, resulting in an obstructive or mechanical shock.
    [Show full text]
  • Characterization, Prevalence, and Risk Factors of Spontaneous And
    Louisiana State University LSU Digital Commons LSU Doctoral Dissertations Graduate School 2013 Characterization, prevalence, and risk factors of spontaneous and experimental atherosclerosis and vascular imaging in psittaciformes Hugues Beaufrère Louisiana State University and Agricultural and Mechanical College, [email protected] Follow this and additional works at: https://digitalcommons.lsu.edu/gradschool_dissertations Part of the Veterinary Medicine Commons Recommended Citation Beaufrère, Hugues, "Characterization, prevalence, and risk factors of spontaneous and experimental atherosclerosis and vascular imaging in psittaciformes" (2013). LSU Doctoral Dissertations. 1598. https://digitalcommons.lsu.edu/gradschool_dissertations/1598 This Dissertation is brought to you for free and open access by the Graduate School at LSU Digital Commons. It has been accepted for inclusion in LSU Doctoral Dissertations by an authorized graduate school editor of LSU Digital Commons. For more information, please [email protected]. CHARACTERIZATION, PREVALENCE, AND RISK FACTORS OF SPONTANEOUS AND EXPERIMENTAL ATHEROSCLEROSIS AND VASCULAR IMAGING IN PSITTACIFORMES A Dissertation Submitted to the Graduate Faculty of the Louisiana State University and Agricultural and Mechanical College in partial fulfillment of the requirements for the degree of Doctor of Philosophy in The Department of Veterinary Clinical Sciences by Hugues Beaufrère Dr.Med.Vet., University of Lyon, France, 2006 Diplomate ABVP – Avian Practice, 2012 Diplomate ECZM (Avian), 2012 May 2013 A Mélanie, qui élève mon cœur. ii ACKNOWLEDGEMENTS First and foremost, I would like to express my thanks to my mentors, Drs. Thomas Tully and Javier Nevarez. Their help, guidance, and trust were instrumental in the completion of my program and these research projects. They promoted unique opportunities at LSU that were far beyond what was just required to succeed in this program.
    [Show full text]
  • Cardiac Arrhythmias in Acute Coronary Syndromes: Position Paper from the Joint EHRA, ACCA, and EAPCI Task Force
    FOCUS ARTICLE Euro Intervention 2014;10-online publish-ahead-of-print August 2014 Cardiac arrhythmias in acute coronary syndromes: position paper from the joint EHRA, ACCA, and EAPCI task force Bulent Gorenek*† (Chairperson, Turkey), Carina Blomström Lundqvist† (Sweden), Josep Brugada Terradellas† (Spain), A. John Camm† (UK), Gerhard Hindricks† (Germany), Kurt Huber‡ (Austria), Paulus Kirchhof† (UK), Karl-Heinz Kuck† (Germany), Gulmira Kudaiberdieva† (Turkey), Tina Lin† (Germany), Antonio Raviele† (Italy), Massimo Santini† (Italy), Roland Richard Tilz† (Germany), Marco Valgimigli¶ (The Netherlands), Marc A. Vos† (The Netherlands), Christian Vrints‡ (Belgium), and Uwe Zeymer‡ (Germany) Document Reviewers: Gregory Y.H. Lip (Review Coordinator) (UK), Tatjania Potpara (Serbia), Laurent Fauchier (France), Christian Sticherling (Switzerland), Marco Roffi (Switzerland), Petr Widimsky (Czech Republic), Julinda Mehilli (Germany), Maddalena Lettino (Italy), Francois Schiele (France), Peter Sinnaeve (Belgium), Giueseppe Boriani (Italy), Deirdre Lane (UK), and Irene Savelieva (on behalf of EP-Europace, UK) Introduction treatment. Atrial fibrillation (AF) may also warrant urgent treat- It is known that myocardial ischaemia and infarction leads to severe ment when a fast ventricular rate is associated with hemodynamic metabolic and electrophysiological changes that induce silent or deterioration. The management of other arrhythmias is also based symptomatic life-threatening arrhythmias. Sudden cardiac death is largely on symptoms rather than to avert
    [Show full text]